| First Author | Paez Espinosa EV | Year | 2012 |
| Journal | Biochem Biophys Res Commun | Volume | 417 |
| Issue | 2 | Pages | 853-6 |
| PubMed ID | 22206677 | Mgi Jnum | J:180287 |
| Mgi Id | MGI:5306062 | Doi | 10.1016/j.bbrc.2011.12.058 |
| Citation | Paez Espinosa EV, et al. (2012) Mouse transient receptor potential channel 6: Role in hemostasis and thrombogenesis. Biochem Biophys Res Commun 417(2):853-6 |
| abstractText | Although changes in the intracellular levels of calcium (Ca(2+)) are a central step in platelet activation, the underlying mechanism of Ca(2+) entry is still unclear. Previous studies have demonstrated that TRPC6, a member of the canonical transient receptor potential channel (TRPC) family is expressed in platelets in a significant amount, and is predominantly found on the plasma membrane. Based on these considerations, we hypothesized that TRPC6 plays a critical role in platelet function. To characterize the role of TRPC6 in platelet function in vivo, we employed a genetic approach, subjecting TRPC6 knockout mice to the tail bleeding time test and a carotid artery injury thrombosis model. We found that TRPC6-deficient animals displayed a prolonged bleeding time, and an increased time for occlusion of the injured carotid artery, compared to their wild-type littermates. Taken together, our data demonstrate for the first time, that TRPC6 deletion in mice results in defects in hemostasis and protection against thrombogenesis, suggesting a vital role in platelet function. Furthermore, TRPC6 may define a new therapeutic target for managing multiple thrombosis-based disorders. |
